Effects of steroid treatment on release of cardiac myosin light chain II in acute myocardial infarction in dogs.
Effects of steroid treatment on release of cardiac myosin light chain II in acute myocardial infarction in dogs.
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类固醇治疗对犬急性心肌梗死心肌肌球蛋白轻链 II 释放的影响。
DOI：
10.1016/0002-9149(84)90331-x
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发表时间：
1984
影响因子：
2.8
通讯作者：
Y. Yazaki
中科院分区：
文献类型：
--
作者：
R. Nagai;M. Isobe;C. Chiu;K. Yamaoki;Y. Ohuchi;S. Ueda;K. Imataka;Y. Yazaki
本文观察了甲基强的松龙琥珀酸钠（MP）对实验性心肌梗塞（MI）心肌肌球蛋白轻链Ⅱ（LC Ⅱ）释放的影响。通过结扎第一对角分支以外的冠状动脉左前降支，在清醒的闭胸犬中产生急性MI。在MI前和MI后24小时静脉注射MP 30 mg/kg。MI后，连续测定血清中的LCII水平直至240小时。MI后10天，通过组织学方法确定MI大小。在MP组中，72小时内血清中的LCII水平低于对照组，并且3天的累积LCII释放从530 ± 159 ng/ml（平均值±标准差）降低至310 ± 101 ng/ml（p < 0.001）。然而，峰值LCII水平出现较晚（对照组vs MP，63 ± 27 vs 122 ± 25小时，p < 0.001），并且MP治疗10天的峰值LCII水平和累积LCII释放没有降低。MP也未减少MI大小（左心室的11.0 ± 4.4% vs 11.8% ± 4.5%，差异不显著）。由于LCII的消失速度很快，不受MP的影响，这些结果表明，急性MI后早期MP治疗延迟了肌球蛋白丝的分解，但不能阻止它。
The effect of methylprednisolone sodium succinate (MP) on release of myosin light chain II (LCII) from the myocardium was studied In experimental myocardial infarction (MI). Acute MI was produced in conscious, closed-chest dogs by ligating the left anterior descending coronary artery beyond the first diagonal branch. MP, 30 mg/kg, was administered intravenously just before and 24 hours after MI. After MI, LCII levels in the serum were determined serially up to 240 hours. MI size was determined histologically 10 days after MI. In the MP group, LCII levels in the serum within 72 hours were lower than in the control, and cumulative LCII release for 3 days decreased from 530 ± 159to310 + 101 ng/ml (mean ± standard deviation) (p < 0.001). However, the peak LCII level appeared later (control vs MP, 63 ± 27 vs 122 ± 25 hours, p < 0.001), and the peak LCII level and cumulative LCII release for 10 days were not decreased by MP treatment. MI size also was not reduced by MP (11.0 ± 4.4% vs 11.8% ± 4.5% of the left ventricle, difference not significant). Since the rate of disappearance of LCII is rapid and was not affected by MP, these results suggest that MP treatment early after acute MI delays breakdown of myosin filaments, but cannot prevent it.